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R D Steele

Publications and source records attributed to R D Steele.

At least 19 recordsLinked to original sources
PubMed2002

The anatomical relationship of the aortic bifurcation to the lumbar vertebrae: a MRI study.

The objective of this study was to determine the level of the aortic bifurcation in relation to the lumbar spine by MRI and the effect of lumbosacral anomalies on the aortic bifurcation. A prospective study of 441 patients was performed. Sagittal MR images of the entire spine were obtained along with the standard protocol for imaging of the lumbar spine. The vertebrae were counted caudally from C2 instead of cranially from the presumed L5 vertebra. The aortic bifurcation in relation to the lumbar vertebrae was determined. The aorta bifurcated at the L4 vertebral body in 67% of cases. In patients with sacralization of L5 the aortic bifurcation was at the L3 vertebral body in 59%. In those patients with lumbarization of S1 the aorta bifurcated at the level of the L4 vertebral body in 40% and at the L4/5 disc space in 33%. There was no demographic variation of the aortic bifurcation in relation to age or sex. The aorta bifurcated at L4 in two-thirds of cases and was variably located in the remaining third. The stability of this as a landmark is disturbed by the significant high incidence of lumbosacral transitional segments.

Adolescent↗
PubMed1999

Improving outcomes for persons with aphasia in advanced community-based treatment programs.

BACKGROUND AND PURPOSE: Studies have yet to document that community-based aphasia treatment programs routinely produce results comparable or superior to published research protocols. We explore this issue here in an outcome study of individuals with aphasia enrolled in 2 community-based, comparably managed and equipped therapy programs, which use a specially designed computer-based tool that is employed therapeutically in adherence to an extensive, detailed, and formally trained patient care algorithm. METHODS: Patients (n=60) were assessed before and after treatment with standardized instruments at both the impairment and the disability levels. Pretreatment and posttreatment means were calculated and compared, with statistical significance of differences established with the use of 1-tailed matched t tests. One-way ANOVAs were used to analyze the comparability of patient performance changes among various subgroups, eg, patients in acute versus chronic stages of aphasia, patients by aphasia diagnostic type at start of care, patients by severity level at start of care, and patients by treatment location. RESULTS: Analysis shows that patients spanned a wide range of aphasia diagnostic types, impairment severity levels at start of care, and times after onset. Patients' mean performance scores improved significantly in response to treatment in all measures assessed at both the impairment level and the functional communication level. Mean overall improvements ranged from 6.6% to 19.8%, with statistical significance ranging from P=0.0006 to P<0.0001. ANOVAs revealed no significant differences between improvements in patients in the acute versus chronic stages of aphasia, between those at different impairment severity levels at start of care, between those treated at different locations, or, at the functional level, between those with different diagnostic types of aphasia at start of care. CONCLUSIONS: Measures of both language impairment and functional communication can be broadly, positively, and significantly influenced by therapy services that are delivered to persons with aphasia in these community-based programs. The significant improvements are shown to be available to individuals with chronic as well as acute aphasia and independent of diagnostic type of aphasia, impairment severity at start of care, or geographic program location.

Adult↗
PubMed1997

Promoting recovery in chronic aphasia with an interactive technology.

OBJECTIVE: To assess chronic aphasic patients' responses to resumption of therapy using an innovative, computer-based treatment system. DESIGN: Patients were assessed pretreatment and posttreatment using standardized assessment tools. Pretreatment and posttreatment performance score means were computed and compared, with statistical significance of the differences established using a one-tailed, matched t test. SETTING: The work was conducted at (1) a Veterans Affairs medical center participating in treatment research and (2) a regional aphasia center delivering therapy services for reimbursement. PATIENTS: Chronic aphasic patients (n = 23) from 6 months to more than 15 years postonset were enrolled in the study. They included a wide range of types and severities of aphasia, and all had received traditional speech-language therapy services earlier. INTERVENTIONS: All patients were treated in 1-hour clinical sessions by speech-language pathologists using the designated computer-based treatment system. All but one of the patients had access to the computer-based treatment system at home for practice between clinical therapy sessions. MAIN OUTCOME MEASURES: The outcome measures used were (1) the Porch Index of Communicative Ability (PICA), (2) the Boston Naming Test (BNT), (3) the Western Aphasia Battery (WAB), and (4) the Boston Diagnostic Aphasia Examination (BDAE). RESULTS: The majority of patients improved significantly in multiple modalities as assessed by these instruments. CONCLUSIONS: Specific measures of language function can be broadly, positively, and significantly influenced by computer-based language therapy in chronic aphasia.

Adult↗
PubMed1997

24-hour radiology.

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Medical Staff, Hospital↗
PubMed1996

Quantification of the carbon flow through the folate-dependent one-carbon pool using radiolabeled histidine: effect of altered thyroid and folate status.

Hyperthyroidism and folate deficiency are known to alter the concentration of hepatic folate pools and the activity of a number of enzymes related to one-carbon metabolism. To evaluate the physiological significance of this relationship on a functional basis, we have developed and utilized an in vivo tracer kinetic technique to quantify the carbon flow through the one-carbon pool as a function of thyroid and folate status. Control, hyperthyroid, and folate-restricted rats were continuously infused with L-[ring-2-14C]histidine to measure the oxidative flow of carbon from histidine through the one-carbon pool to CO2. As expected, the hepatic activities of a number of enzymes involved in the catabolism of histidine to CO2 were markedly decreased in hyperthyroid (histidase, 69%; urocanase, 30%; 10-formyltetrahydrofolate dehydrogenase, 65%) and folate-restricted (10-formyltetrahydrofolate dehydrogenase, 44%) rats. In addition, folate-restricted animals exhibited a 63% decrease in the hepatic concentration of total reduced folates. However, tracer kinetic analysis indicated an enhanced catabolism of histidine: the carbon flux from histidine to CO2 was increased approximately threefold in hyperthyroid rats and twofold in folate-restricted animals. Thus, in the case of hyperthyroidism and dietary folate restriction, changes in static measurements such as metabolite concentrations and enzyme activities do not reflect the dynamic tracer kinetic assessment of the carbon flux that is actually occurring in vivo. The kinetic data also demonstrate that the percentage of total entry into the 10-formyltetrahydrofolate pool originating from histidine catabolism was almost threefold greater compared to 5-methyltetrahydrofolate pool.

Animals↗
PubMed1996

Methotrexate alters carbon flow through the hepatic folate-dependent one-carbon pool in rats.

The chemotherapeutic value of methotrexate resides in its ability to perturb folate-dependent one-carbon metabolism and subsequently inhibit DNA synthesis. To assess the functional effect of methotrexate on hepatic one-carbon metabolism, we have developed and applied tracer kinetic techniques in vivo to quantify the carbon flux through the folate-dependent one-carbon pool in rats. Following a 7-day treatment period with methotrexate (0.2 mg/kg body weight), the tracers L-[ring-2-14C] histidine and L-[methyl-3H] methionine were simultaneously infused into control and methotrexate-treated rats. Methotrexate treatment decreased hepatic tetrahydrofolate, methyltetrahydrofolate, and formyltetrahydrofolate, concentrations by 63, 83, and 58%, respectively. Furthermore, the enzymatic activity of 10-formyltetrahydrofolate dehydrogenase, the terminal enzyme in the catabolism of the ring-2-carbon of histidine to CO2, was diminished by 32% in methotrexate-treated animals. These changes in enzyme activity and folate coenzyme concentrations did not result in a significant decrease in the oxidative flow of carbon from histidine to CO2 in methotrexate-treated rats compared to control animals (2.40 and 3.22 micromol/h/kg3/4, respectively). Oxidative carbon flow was reflective of tetrahydrofolate and formyltetrahydrofolate pools when expressed as a percent of total folate: neither coenzyme pool was diminished as a result of methotrexate treatment. In contrast, the reductive carbon flux through the one-carbon pool from histidine to methionine was significantly decreased 59% in methotrexate-treated (7.63 micromol/h/kg3/4) versus control rats (18.73 micromol/h/kg3/4)). Likewise, methyltetrahydrofolate, as a percent of total folate, was reduced 51% in methotrexate-treated rats. Consequently, total measured carbon flow (oxidative+reductive) was 54% lower in rats subjected to subchronic methotrexate treatment. These tracer kinetic experiments quantitatively demonstrate the extent to which methotrexate alters the actual carbon flow through the hepatic folate-dependent one-carbon pool, primarily directed at diminishing the reductive carbon flow towards methyltetrahydrofolate and methionine synthesis.

Animals↗
PubMed1996

Carbon flow through the hepatic folate-dependent one-carbon pool is not altered in vitamin A-deficient rats.

Vitamin A status can influence a number of enzymes and coenzymes involved in folate-dependent one-carbon metabolism as well as subsequent methyl group metabolism. Tracer kinetic techniques were used in the present study to assess the physiological importance of vitamin A deficiency on the de novo synthesis of methionine via the hepatic folate-dependent one-carbon pool. Vitamin A-deficient (0 retinol equivalents (RE) retinyl palmitate/g diet) rats were fed their respective diet for 11 wk, whereas control rats (1.2 RE retinyl palmitate/g diet) were food restricted to match the growth rate exhibited by the vitamin A-deficient group. After the dietary treatment period, duodenal cannulated rats were continuously infused with L-[3-(14)C] serine and L-[methyl-(3)H] methionine until a plateau specific radioactivity was exhibited with respect to the hepatic serine and methionine pools, indicating a steady state had been achieved. The hepatic concentration of both S-adenosylmethionine a S-adenosylhomocysteine were elevated in vitamin A-deficient rats. However, Vitamin A-deficient rats exhibited similar kinetic values compared with control rats fed a vitamin A-sufficient diet. The irreversible loss rate of hepatic serine and methionine, the transfer quotient from serine to methionine and the folate-dependent flow of carbon to methionine from serine were unaffected by vitamin A status. These studies demonstrate that vitamin A deficiency does not affect the reductive carbon flow from serine to methionine because the ability to generate methionine via remethylation of homocysteine with the carbon group originating from serine was not altered in vitamin A-deficient rats. Furthermore, the data illustrate the importance of using tracer kinetic techniques to quantify metabolic flux under steady-state conditions in vivo, thereby evaluating the consequences of an abnormal condition on a physiological and functional basis.

Animals↗
PubMed1995

Cloning and characterization of rat cysteine sulfinic acid decarboxylase.

Cysteine sulfinic acid decarboxylase (CSAD) is a key enzyme in taurine biosynthesis. CSAD activity and enzyme protein concentration are both repressed by the action of the steroid family hormones triiodothyronine and estrogen. To characterize this suppression, a cDNA clone for CSAD was isolated from a rat liver cDNA expression library using polyclonal antibodies to CSAD. The cDNA was sequenced in its entirety and confirmed to be a clone of CSAD. In a Northern blot comparing liver and kidney RNA of male and female rats, the CSAD cDNA probe detected a 2.5 kb mRNA band which was present at levels corresponding to the concentration of enzyme protein. Hyperthyroidism decreased CSAD mRNA as compared to euthyroid controls, providing evidence that negative regulation of CSAD activity occurs at the level of mRNA.

Amino Acid Sequence↗
PubMed1993

13-cis-retinoic acid and hepatic steatosis in rats.

The effect of administration of 13-cis-retinoic acid (100 mg/kg diet) on lipid metabolism was examined in male rats fed either a 20% casein + 0.3% methionine diet, a 20% casein diet, a 10% casein + 0.3% methionine diet, or a 10% casein + 0.6% methionine diet for 10 days. Hepatic triglyceride concentrations of rats fed either 10% casein diet were 3-fold greater than animals receiving diets containing 20% casein. The addition of 13-cis-retinoic acid to the diet further increased the total hepatic lipid (43-56%) and triglyceride (approximately 2-fold) concentrations in rats fed the 10% casein diets. 13-cis-Retinoic acid supplementation did not alter the total liver lipid or triglyceride concentrations in rats fed either of the 20% casein diets. Thus, under specific dietary conditions, the administration of 13-cis-retinoic acid resulted in a marked accumulation of hepatic lipids which did not appear to be related to the total methionine content of the diet nor to the hepatic concentrations of S-adenosylmethionine and glutathione. In addition, all four groups of 13-cis-retinoic acid-fed rats exhibited elevations in the concentration of serum triglycerides, and 10-20% reductions in serum cholesterol concentrations.

Animals↗
PubMed1992

Quantification of cysteine sulfinic acid decarboxylase in male and female rats: effect of adrenalectomy and methionine.

Hepatic cysteine sulfinic acid decarboxylase (EC 4.1.1.29) activity has been reported to decrease in response to both L-methionine (Met) feeding and adrenalectomy in rats. A series of experiments was conducted to (a) determine if CSAD depression was evident in female rats fed a methionine-supplemented diet; and (b) determine if adrenal hormones mediated the response of CSAD to dietary methionine. Cysteine sulfinic acid decarboxylase (CSAD) activity was measured in livers of male and female rats fed a methionine-supplemented diet. In female rat liver, CSAD activity was only 25% of the activity measured in livers of male rats. Hepatic enzyme activity in male rats fed a casein-based basal diet containing 0.6% L-methionine was 2.5-fold higher than activity in male rats fed a methionine-supplemented diet containing 1.35% L-methionine (+Met). Similarly, enzyme activity in livers of female rats fed the basal diet was 1.7-fold higher than in female rats fed a methionine-supplemented diet. CSAD activity in adrenalectomized (ADX) male rats fed the basal diet was depressed (990 +/- 120 nmol/min.g liver) compared to activity in intact controls (2347 +/- 89) and sham controls (2040 +/- 143) fed the basal diet. CSAD activity was further depressed in ADX, intact controls, and sham controls fed +Met. Immunochemical detection and quantification of CSAD protein in rat liver demonstrated that changes in CSAD protein were consistent with the observed decreased enzyme activity in female rats, ADX rats, and rats fed +Met. S-Adenosylmethionine and S-adenosylhomocysteine concentrations tended to increase in livers of rats fed +Met. ADX rats fed +Met had the greatest increase in S-adenosylmethionine and S-adenosylhomocysteine concentrations. The depression in hepatic CSAD observed after feeding +Met to rats does not appear to involve adrenal function.

Adrenalectomy↗
PubMed1992

Variations in S-adenosylmethionine, S-adenosylhomocysteine and adenosine concentrations in rat liver.

The hepatic concentrations of S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH) and adenosine (Ado) in the rat were examined diurnally and as a function of fasting. Ado concentrations increased continuously throughout the fasting period; concentrations after 2 days of fasting were 7.5-fold higher than control values. Diurnally, the concentration of Ado was highest during the light hours. SAM and the ratio of SAM/SAH were reduced greater than 50% due to fasting and exhibited a significant daily rhythm which appeared to be related to dietary methionine availability. Hepatic SAM concentrations decreased continuously during the light hours and increased during the dark period to levels 7.3-fold greater than the lowest light values. The concentration of SAH was altered in a similar fashion yet to a much lesser degree such that the ratio of SAM/SAH paralleled the changes in the concentration of SAM. The SAM/SAH ratio exhibited a 4.5-fold difference between the peak and nadir values.

Adenosine↗
PubMed1991

Cysteine sulfinic acid decarboxylase activity in response to thyroid hormone administration in rats.

The modulation of hepatic and renal cysteine sulfinic acid decarboxylase (EC 4.1.1.29) activities by triiodothyronine (T3) was studied in a series of experiments. In a dose--response study, hepatic cysteine sulfinic acid decarboxylase activity (CSAD) was depressed by 65% and renal activity was increased threefold in rats injected with 100 micrograms T3/100 g body wt for 7 days when compared to rats injected with 0.3 micrograms T3/100 g body wt. Western blot analysis indicated that these changes in CSAD activity were due to changes in the quantity of CSAD protein. Changes in hepatic and renal activities were not evident until 24 h after T3 administration. In response to T3 clearance, hepatic and renal CSAD activities approached euthyroid values 4-7 days after cessation of T3 injections although serum T3 concentrations were no different from euthyroid values 48 h after T3 injections were stopped. These data indicate that thyroid hormone effects persist after T3 clearance. The response of CSAD to thyroid status may be related to its role in taurine biosynthesis.

Animals↗
PubMed1991

13-cis-retinoic acid alters methionine metabolism in rats.

The effect of dietary 13-cis-retinoic acid (CRA) on hepatic methionine metabolism was examined in young male rats. Rats were fed a 10% casein diet (controls) or this diet supplemented with L-methionine (10 g/kg diet), with or without the addition of CRA (100 mg/kg diet), for 10 d. Methionine-supplemented rats exhibited 7.3- and 1.7-fold greater concentrations of hepatic S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), respectively, relative to controls, which resulted in a 4.9-fold greater SAM:SAH ratio. Likewise, hepatic methionine and taurine concentrations were 6.9- and 4.3-fold greater, respectively, in methionine-supplemented rats than in controls. The addition of CRA to the methionine-supplemented diet prevented the elevations in the hepatic methionine concentration and the SAM:SAH ratio, whereas taurine levels were greater than in methionine-supplemented rats. In rats pretreated with the methionine-supplemented diet, a reduction in the SAM:SAH ratio occurred within 2 d following the addition of CRA to the methionine-supplemented diet. Rats receiving the methionine-supplemented diet exhibited 9.2- and 3.7-fold greater urinary taurine and inorganic sulfate excretions, respectively, relative to controls. Addition of CRA to the methionine-supplemented diet significantly reduced sulfate excretion by 21%. These findings indicate that dietary CRA has the ability to alter the catabolism of methionine and subsequently influence hepatic transmethylation as reflected by the SAM:SAH ratio.

Animals↗
PubMed1991

Dietary sulfur amino acid modulation of cysteine sulfinic acid decarboxylase.

Male rats were fed sulfur and nonsulfur amino acid-supplemented diets, and the response of cysteine sulfinic acid decarboxylase (CSAD) activity was determined. After adaptation to a casein-based basal diet, rats were fed diets containing additions of L-methionine. Hepatic CSAD activity decreased in a dose-dependent manner. Significant depression of CSAD activity in liver was evident within 24 h of feeding rats a methionine-supplemented diet. Depression of enzyme activity was reversed upon refeeding the basal diet. After rats were fed diets supplemented with methionine, cystine, homocystine, S-methyl-L-cysteine, phenylalanine, leucine, or ethionine for 14 days, hepatic CSAD activity in rats fed S-methyl-L-cysteine-, phenylalanine-, or leucine-supplemented diets was not depressed compared with activity in rats fed a basal diet. In contrast, CSAD activity in livers of rats fed cystine-, homocystine-, methionine-, or ethionine-supplemented diets was 60, 40, 40, and 8%, respectively, of the activity in livers from control rats. Immunochemical detection and quantification of CSAD protein in rat liver indicated that CSAD protein concentration was correlated to CSAD activity. CSAD activity may be specifically regulated by sulfur amino acids metabolized by the S-adenosylmethionine-dependent pathway of methionine metabolism.

Amino Acids↗
PubMed1989

Quantitation of carbon flow through the hepatic folate-dependent one-carbon pool in rats.

The quantitation of carbon flow through the folate-dependent one-carbon pool in regard to the synthesis of methionine from the amino acid precursor, serine, was determined in rat liver. Utilizing duodenal cannulated rats and in vivo tracer kinetic techniques where [3-14C]serine was continuously infused at a rate of 3.32 microCi/h, a steady-state (plateau) specific radioactivity was achieved within 200 min from the onset of the infusion period. This resulted in an irreversible loss rate of 431 +/- 12 mumol/h for hepatic serine. In conjunction with the specific radioactivity measurements of hepatic methionine, the percentage of the total entry into the hepatic methionine methyl carbon pool that came from serine (i.e., transfer quotient) was calculated to be 51.7 +/- 5.2%. Similar experiments utilizing [methyl-3H]methionine as the infusate resulted in a value of 112 +/- 6 mumol/h for the irreversible loss rate of hepatic methionine. Using the irreversible loss rate of methionine and the transfer quotient to methionine from serine, the flux of the beta-carbon of serine to remethylate homocysteine and generate methionine was calculated to be 57.9 mumol/h. These results not only present a methodology for the determination of folate-dependent carbon flow in vivo, but also demonstrate the high degree to which the homocysteine moiety of methionine is conserved in vivo to meet the methylation requirements in the rat.

Animals↗